Acute severe asthma: signs and emergency care

Acute severe asthma is a life-threatening exacerbation with rapidly worsening airflow obstruction, respiratory failure, and the risk of respiratory arrest. It is characterized by a sharp increase in shortness of breath, wheezing or "silent lung," a drop in oxygen saturation, and respiratory muscle fatigue; delayed treatment is associated with a high mortality rate. The diagnosis is clinical and does not require waiting for laboratory results: treatment is initiated immediately, along with ongoing testing. [1]

The key goal in the first minutes is to establish airway patency with high-dose short-acting β2-agonists, add ipratropium, administer systemic glucocorticoids early, titrate oxygen to target levels, and, if necessary, consider intravenous magnesium sulfate. Decisions to escalate respiratory support are made promptly. [2]

Even with normal oxygen saturation, a severe exacerbation can quickly decompensate due to dynamic hyperinflation and respiratory muscle fatigue. Therefore, continuous monitoring of respiration, heart rate, accessory muscle function, and level of consciousness is as important as pharmacotherapy. [3]

Epidemiology

Asthma exacerbations remain a leading cause of emergency room visits and hospitalizations in adults and children; the proportion of severe episodes is higher in patients with poor symptom control, low adherence, and lack of anti-inflammatory background therapy. GINA-2024 emphasizes that in adults and adolescents, therapy with short-acting β2-agonists alone is no longer acceptable due to the increased risk of severe exacerbations. [4]

In intensive care units, mortality rates are higher when invasive ventilation is required than with conservative management; early implementation of a "bundle" of measures in the emergency department reduces the incidence of mechanical ventilation and complications. Viral waves and concomitant respiratory pathology contribute most to the burden of severe exacerbations. [5]

Reasons (triggers)

Classic triggers include viral respiratory infections, allergens (pollen, house mites, animals), air pollution and tobacco smoke, cold air, physical activity, and drug triggers (non-selective β-blockers, aspirin/NSAIDs in aspirin-induced respiratory disease). Severe exacerbations are often precipitated by a sharp reduction in the dose of controller therapy or its discontinuation. [6]

Anaphylaxis and the “aspirin triad” are particularly dangerous – here the algorithm is supplemented with immediate intramuscular adrenaline and anti-shock measures. [7]

Risk factors for severe disease and death

High risk: previous intubation/mechanical ventilation or hospitalization for asthma in the past year, frequent use of SABA (e.g., more than 3 cylinders per year), no/low doses of inhaled corticosteroids, poor inhalation technique and low adherence, underlying psychosocial vulnerability, pregnancy, obesity, active smoking. Identification of these factors in the emergency department determines a more aggressive surveillance strategy. [8]

Pathogenesis

The underlying cause is an acute increase in bronchial wall inflammation, mucosal edema, mucus plugs, and severe bronchospasm, which creates severe expiratory obstruction. Dynamic hyperinflation occurs with increased intrathoracic pressure, decreased venous return, and the risk of hypotension; hypercapnia often precedes hypoxemia. Respiratory muscle fatigue and a "quiet" chest sound ("silent lung") are harbingers of respiratory collapse. [9]

Symptoms

Increasing shortness of breath, difficulty exhaling, inability to speak in sentences, use of accessory muscles, tachycardia, sweating, anxiety, or, conversely, decreased consciousness. Auscultation reveals loud whistles or their disappearance with a "silent lung." Pulse oximetry and respiratory rate do not always reflect the severity of air trapping—a comprehensive clinical assessment is essential. [10]

Forms and stages (severity assessment in the emergency department)

The severity of an exacerbation is determined by clinical presentation, peak flow/spirometry (if feasible), and blood gas measurements. Signs of a life-threatening exacerbation include confusion, "silent lung," bradycardia, oxygen saturation <90% on air, PaCO₂ ≥45 mmHg, and severe fatigue—indications for immediate escalation of support and possible intubation. [11]

Table 1. Criteria for severe/life-threatening exacerbation (total)

Block	Heavy	Threat to life
Speech/behavior	Words/short phrases	Confusion, "dumb" behavior
Breath	Respiratory rate >25-30, use of accessory muscles	"Silent lung", fatigue
SpO₂ (in air)	<92-94%	<90%
Blood gases	Norm/onset of hypercapnia	PaCO₂ ≥45 mmHg
Peak flow	<50% of expected or better	Not implemented
Based on GINA-2024 and critical reviews.[12]

Complications and consequences

Early: hypoxemia, hypercapnia, arrhythmias (β2-agonists, hypokalemia), pneumothorax/pneumomediastinum (barotrauma during mechanical ventilation, cough), aspiration. Late: rhabdomyolysis and hypophosphatemia with β2-agonists, infectious complications with prolonged ventilation. Every additional hour before systemic steroids and adequate bronchodilators are administered increases the risk of mechanical ventilation and prolonged hospitalization. [13]

Diagnostics

At a minimum, in the first minutes: pulse oximetry with oxygen titration, ECG monitoring, complete blood count/electrolytes in severe cases (potassium, glucose monitoring), venous/arterial blood gases if there are signs of fatigue or treatment failure. Chest X-ray - if complications or an atypical picture are suspected; routine antibiotics and searches for bacterial infection are not indicated without obvious signs. Peak expiratory flow rate - when safe. [14]

Differential diagnosis

Anaphylaxis, exacerbation of chronic obstructive pulmonary disease, pulmonary embolism, pneumothorax, pulmonary edema, vocal fold dysfunction, foreign body, hyperventilation crisis. In doubtful cases, the diagnosis is based on the medical history, triggers, objective data, and the dynamics of therapy. [15]

Treatment (detailed algorithm for emergency care)

Oxygen. Target SpO₂ 93-95% (94-98% for children) using titrated oxygen (cannula/mask/VPN if needed). Avoid hyperoxia. [16]

Bronchodilation. Continuous or frequent nebulizations of SABA (salbutamol 2.5-5 mg every 10-20 minutes for the first hour, in severe cases - almost continuously via a nebulizer or metered-dose inhaler with a spacer in equivalent doses) + ipratropium bromide 0.5 mg every 20 minutes × 3 in the first hour. The combination of SABA + ipratropium in the acute period reduces the risk of hospitalization and mechanical ventilation. [17]

Systemic glucocorticoids (as soon as possible). Preferably within the first 30-60 minutes: prednisolone orally 40-50 mg (adults) or methylprednisolone intravenously 40-80 mg if oral administration is not possible; in children, based on weight. Duration is usually 5-7 days (adults) without the need for "tapering" with short courses. Early administration reduces the risk of hospitalization and relapse. [18]

Intravenous magnesium sulfate. Indicated for severe/refractory attacks after the initial hour of therapy: 2 g intravenously over 20 minutes (children 25-50 mg/kg, max 2 g). Reduces the risk of hospitalization in patients with severe obstruction; nebulized MgSO₄ is not routinely recommended. [19]

Adrenaline (epinephrine). Only for anaphylaxis, angioedema, or anaphylactoid reactions: 0.3–0.5 mg intramuscularly (1:1000) into the lateral thigh, repeated every 5–10 minutes as indicated. [20]

What is NOT routinely recommended: Theophylline/aminophylline, sedatives and opioids (which worsen hypoventilation), helium-oxygen without clear indications, and routine antibiotics. The decision on nebulized budesonide as an adjunct to systemic steroids is based on local protocols. [21]

Respiratory support. Non-invasive ventilation (NIV) - only in carefully selected patients under supervision; at the first signs of fatigue/hypercapnia, failure of non-invasive support - early intubation by an experienced team. Mechanical ventilation: low frequency, small volumes (6-8 ml/kg), prolonged expiration, acceptable hypercapnia, plateau pressure control, prevention of barotrauma and dynamic hyperinflation. Rarely, in case of refractory hypercapnia - extracorporeal CO₂ removal/VV-ECMO in experienced centers. [22]

Table 2. The "bundle" of emergency care in the first 60 minutes

Component	Action
Monitoring	SpO₂, RR/HR, BP, level of consciousness, frequent reassessment
Oxygen	Titrate to SpO₂ 93-95%
Inhalations	Continuous/frequent SABA + ipratropium (first hour)
Steroids	Systemic glucocorticoids in the first 30-60 minutes
MgSO₄	2 g intravenously for severe/resistant attacks
Escalation	VPNK/NVL → ALV for fatigue, hypercapnia, "silent lung"
The algorithm summarizes the provisions of GINA-2024 and critical reviews. [23]

Prevention (after the attack has been stopped)

Before discharge, it is essential to: provide a written action plan, check inhalation technique and adherence, prescribe anti-inflammatory background therapy with an inhaled corticosteroid (in adults/adolescents, access to an as-needed regimen of ICS/formoterol or a regular combination), reduce or eliminate SABA monotherapy, identify and, if possible, eliminate triggers, discuss influenza vaccination, rhinitis/reflux control strategy, and smoking cessation. Follow-up visit - within 2-7 days. [24]

Forecast

The outcome of an exacerbation is determined by the speed of initiation of appropriate therapy, the initial severity, the presence of risk factors, and the quality of secondary prevention. Early administration of systemic steroids, combined inhalations of SABA and ipratropium, and MgSO₄ when indicated, and timely escalation of respiratory support reduce the risk of mechanical ventilation and mortality. In the long term, transition to the GINA-2024 strategy (ICS-containing therapy for all) reduces the incidence of future severe attacks. [25]

FAQ

• When to call an ambulance?

If, despite repeated inhalations of salbutamol (every 10-20 minutes x 1 hour), severe shortness of breath, difficulty speaking, a drop in SpO₂, “dumb” breathing, confusion, or increasing drowsiness persist, this is an emergency. [26]

• Are antibiotics necessary for a severe attack?

No, unless there is obvious evidence of a bacterial infection. Routine antibiotic use during asthma exacerbations does not improve outcomes. [27]

• Magnesium for everyone?

No. Intravenous MgSO₄ is indicated for severe/refractory attacks after the first hour of intensive inhalational therapy and systemic steroids. Nebulized magnesium is not routinely recommended. [28]

• Is it possible to overdo it with salbutamol?

Frequent inhalations in the first 60 minutes is a standardized tactic, but excess SABA outside of a controlled algorithm increases the risk of tachycardia, tremor, hypokalemia, and worse outcomes. Early initiation of steroids and the addition of ipratropium are crucial. [29]

Special considerations

• In severe asthma with very high airway pressures, decreased tidal volume and fluctuating capnographic curves, mechanical ventilation may be difficult.
• Manual ventilation with a low-compliance system may be required, but monitoring airway pressure, particularly inspiratory pressure, is crucial. Airway pressures of up to 30-40 cm H2O may be necessary. Elevated pressures indicate the need for maximal bronchodilator therapy.
• All inhalational anesthetics relax the bronchi and can be useful during severe attacks. Care must be taken to ensure proper drainage of the used gas mixture.
• These children are usually dehydrated, so induction of anesthesia for intubation should be preceded by a 20 ml/kg crystalloid infusion. Slow administration is preferred, but rapid sequence induction may be necessary in fasted patients. Propofol and ketamine are ideal.
• Peak expiratory flow rate (PEF) in children: This is a simple method for measuring airway obstruction, allowing one to determine the severity of the condition. It is measured using a standard Wright peak flow meter.